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5'-adenosine monophosphate-induced hypothermia attenuates brain ischemia/reperfusion injury in a rat model by inhibiting the inflammatory response.

Miao YF, Wu H, Yang SF, Dai J, Qiu YM, Tao ZY, Zhang XH - Mediators Inflamm. (2015)

Bottom Line: Hypothermia treatment is a promising therapeutic strategy for brain injury.Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls.AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Ren Ji Hospital, South Campus, Shanghai Jiao Tong University School of Medicine, Shanghai 201112, China.

ABSTRACT
Hypothermia treatment is a promising therapeutic strategy for brain injury. We previously demonstrated that 5'-adenosine monophosphate (5'-AMP), a ribonucleic acid nucleotide, produces reversible deep hypothermia in rats when the ambient temperature is appropriately controlled. Thus, we hypothesized that 5'-AMP-induced hypothermia (AIH) may attenuate brain ischemia/reperfusion injury. Transient cerebral ischemia was induced by using the middle cerebral artery occlusion (MCAO) model in rats. Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls. AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells. The overall infarct volume was significantly smaller in AIH-treated rats, and neurological function was improved. By contrast, rats with ischemic brain injury that were administered 5'-AMP without inducing hypothermia had ischemia/reperfusion injuries similar to those in euthermic controls. Thus, the neuroprotective effects of AIH were primarily related to hypothermia.

No MeSH data available.


Related in: MedlinePlus

AIH reduces brain infarct volume in the ischemia/reperfusion rat model. TTC staining was used to measure the brain infarct volume 24 h after reperfusion. (a) Representative infarct volume stained with TTC in each group. (b) Average infarct volume in rats treated with 5′-AMP coupled with low Ta. All values are mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.
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fig2: AIH reduces brain infarct volume in the ischemia/reperfusion rat model. TTC staining was used to measure the brain infarct volume 24 h after reperfusion. (a) Representative infarct volume stained with TTC in each group. (b) Average infarct volume in rats treated with 5′-AMP coupled with low Ta. All values are mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.

Mentions: Brain infarct volumes were measured by TTC staining. To determine the effects of AIH on brain ischemic injury, the infarct size due to ischemic insult was calculated using imaging software. Representative images of infarcted areas (white) are shown in Figure 2(a). In the MCAO group, a large infarcted area was predominantly located in the cerebral cortex and the striatum. The normalized infarct volume in the MCAO, NT, and HT(0.5) groups was 42.15 ± 1.78%, 39.39 ± 0.98%, and 32.22 ± 0.65%, respectively. AIH treatment reduced brain infarct volume to 5.33 ± 1.30% (P < 0.05 versus the MCAO, NT, and HT(0.5) groups, Figure 2(b)).


5'-adenosine monophosphate-induced hypothermia attenuates brain ischemia/reperfusion injury in a rat model by inhibiting the inflammatory response.

Miao YF, Wu H, Yang SF, Dai J, Qiu YM, Tao ZY, Zhang XH - Mediators Inflamm. (2015)

AIH reduces brain infarct volume in the ischemia/reperfusion rat model. TTC staining was used to measure the brain infarct volume 24 h after reperfusion. (a) Representative infarct volume stained with TTC in each group. (b) Average infarct volume in rats treated with 5′-AMP coupled with low Ta. All values are mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4385688&req=5

fig2: AIH reduces brain infarct volume in the ischemia/reperfusion rat model. TTC staining was used to measure the brain infarct volume 24 h after reperfusion. (a) Representative infarct volume stained with TTC in each group. (b) Average infarct volume in rats treated with 5′-AMP coupled with low Ta. All values are mean ± SEM. *P < 0.05 compared to the MCAO group, #P < 0.05 compared to the NT group, and &P < 0.05 compared to the HT(0.5) group.
Mentions: Brain infarct volumes were measured by TTC staining. To determine the effects of AIH on brain ischemic injury, the infarct size due to ischemic insult was calculated using imaging software. Representative images of infarcted areas (white) are shown in Figure 2(a). In the MCAO group, a large infarcted area was predominantly located in the cerebral cortex and the striatum. The normalized infarct volume in the MCAO, NT, and HT(0.5) groups was 42.15 ± 1.78%, 39.39 ± 0.98%, and 32.22 ± 0.65%, respectively. AIH treatment reduced brain infarct volume to 5.33 ± 1.30% (P < 0.05 versus the MCAO, NT, and HT(0.5) groups, Figure 2(b)).

Bottom Line: Hypothermia treatment is a promising therapeutic strategy for brain injury.Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls.AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, Ren Ji Hospital, South Campus, Shanghai Jiao Tong University School of Medicine, Shanghai 201112, China.

ABSTRACT
Hypothermia treatment is a promising therapeutic strategy for brain injury. We previously demonstrated that 5'-adenosine monophosphate (5'-AMP), a ribonucleic acid nucleotide, produces reversible deep hypothermia in rats when the ambient temperature is appropriately controlled. Thus, we hypothesized that 5'-AMP-induced hypothermia (AIH) may attenuate brain ischemia/reperfusion injury. Transient cerebral ischemia was induced by using the middle cerebral artery occlusion (MCAO) model in rats. Rats that underwent AIH treatment exhibited a significant reduction in neutrophil elastase infiltration into neuronal cells and matrix metalloproteinase 9 (MMP-9), interleukin-1 receptor (IL-1R), tumor necrosis factor receptor (TNFR), and Toll-like receptor (TLR) protein expression in the infarcted area compared to euthermic controls. AIH treatment also decreased the number of terminal deoxynucleotidyl transferase dUTP nick end labeling- (TUNEL-) positive neuronal cells. The overall infarct volume was significantly smaller in AIH-treated rats, and neurological function was improved. By contrast, rats with ischemic brain injury that were administered 5'-AMP without inducing hypothermia had ischemia/reperfusion injuries similar to those in euthermic controls. Thus, the neuroprotective effects of AIH were primarily related to hypothermia.

No MeSH data available.


Related in: MedlinePlus